Apigenin Attenuates Inflammation in Experimentally Induced Acute Pancreatitis-Associated Lung Injury

Basios, Neofitos; Lampropoulos, Pavlos; Papalois, Αpostolos; Lambropoulou, María; Pitiakoudis, Michael K; Kotini, A; Simopoulos, Constantinos; Tsaroucha, Alexandra

doi:10.3109/08941939.2015.1088603

Cited by 11 publications

(6 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus, the protective effects of UTI on rat lung injury were associated with proteins of the TLR4/MyD88/NF-κB signaling pathway. Discussion 9 ALI, as a common clinical respiratory critical disease, is pulmonary parenchyma injury mainly caused by the interaction of inflammatory mediators and effector cells [21]. At present, effective therapies are still lacking in clinical practice, so it is imperative to seek prevention and treatment measures.…”

Section: Effects Of Uti On Protein Expressions Of Tlr4 Myd88 and Nf-κb In Lung Tissue Of Lps-induced Ratsmentioning

confidence: 99%

Protective effects of ulinastatin on rats with acute lung injury induced by lipopolysaccharide

Lü

Liu

et al. 2021

Bioengineered

View full text Add to dashboard Cite

We aimed to evaluate the protective effects of ulinastatin (UTI) on rats with acute lung injury induced by lipopolysaccharide (LPS) via the Toll like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor-kappa B (NF-κB) signaling pathway. Forty-eight male Wistar rats were randomly divided into model, control, dexamethasone (DXM) and UTI groups. The body weight loss ratio and wet-to-dry weight ratio (W/D) of lung tissue were calculated at 10 h. The permeability of pulmonary vascular endothelium was detected by Evans blue method. Tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-1β levels in bronchial lavage fluid were detected by enzyme-linked immunosorbent assay. Total cells and neutrophils were counted by microscopy. TLR4, MyD88 and NF-κB expressions were detected by Western blotting. Compared with model group, DXM and UTI 2 groups had significantly higher body weights and lower W/D values (P<0.05). In DXM and UTI groups, the lung tissue structure was close to normal, inflammatory cell infiltration was alleviated, and hematoxylin-eosin staining scores were significantly lower than that of model group (P<0.05). Compared with model group, the concentrations of Evans blue, IL-1β, IL-6 and TNF-α levels, and protein expressions of TLR4, MyD88 and NF-κB in DXM and UTI groups decreased significantly (P<0.05). UTI inhibits LPS-induced activation of the TLR4/MyD88/NF-κB signaling pathway, thereby alleviating inflammatory response and protecting against lung injury.

show abstract

Section: Effects Of Uti On Protein Expressions Of Tlr4 Myd88 and Nf-κb In Lung Tissue Of Lps-induced Ratsmentioning

confidence: 99%

Protective effects of ulinastatin on rats with acute lung injury induced by lipopolysaccharide

Lü

Liu

et al. 2021

Bioengineered

View full text Add to dashboard Cite

show abstract

“…The most beneficial aspect of these phytochemicals is the lack of side effects. Therefore, in search of more treatment options for SAP associated ALI, researchers have tested several phytochemicals such as resveratrol [65] and apigenin [66] in experimental models and these phytochemicals have revealed promising protective potential for the treatment of SAP associated ALI.…”

Section: Phytocompounds Used For Treatment Of Sap Associated Lung Infmentioning

confidence: 99%

“…Results indicate improvement of lung tissue damage following apigenin administration. Apigenin reduces most histopathological alterations of the pulmonary tissue and decreases MPO and TNF-α activity [66].…”

Section: Apigeninmentioning

confidence: 99%

Chronic Pancreatitis Associated Acute Respiratory Failure

Anil¹

2017

MOJI

View full text Add to dashboard Cite

“…Studies have shown that children with different degrees of obesity have different degrees of glucose and lipid metabolism disorders. In these cases, as the degree of obesity increases, glucose and lipid metabolism disorders become more aggravated[ 1 ]. Insulin resistance (IR) refers to a decrease in the body's sensitivity to insulin, a decrease in the ability of insulin to lower blood sugar, and an obstacle to the use of glucose by tissues[ 2 ].…”

Section: Introductionmentioning

confidence: 99%

Decabromodiphenyl ether causes insulin resistance and glucose and lipid metabolism disorders in mice

Alimu

Abudureman

Wang³

et al. 2021

WJD

View full text Add to dashboard Cite

BACKGROUND Decabromodiphenyl ether (BDE-209) is the most commonly used brominated flame retardant. Recently, BDE-209 has been suspected of being an environmental risk factor for metabolic diseases such as obesity, insulin resistance (IR), type 2 diabetes mellitus, and hypertension. AIM To investigate the effects of BDE-209 on IR and glucose and lipid metabolism in C57BL/6 mice. METHODS Adult male C57BL/6 mice were randomly divided into high, medium-high, medium, medium-low, and low dose BDE-209 groups, and a control group ( n = 6 per group), which received 1000, 800, 600, 450, 300, and 0 mg/kg BDE-209, respectively. After BDE-209 exposure for 60 d, the mice were fasted overnight, and then sacrificed to obtain tissues. An automatic biochemical analyzer was used to detect serum triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and high density lipoprotein cholesterol (HDL-C); enzyme-linked immunosorbent assay kits were used to detect fasting serum insulin (FINS), leptin (LEP), and adiponectin (Adp) levels; a blood glucose meter was used to detect fasting blood glucose (FBG). Morphological changes of the liver were observed by hematoxylin and eosin staining. Real-time quantitative polymerase chain reaction and Western blot were used to determine the messenger ribonucleic acid (mRNA) and protein levels, respectively, of LEP, Adp, and peroxisome proliferators activated receptor-γ (PPARγ) in mouse liver and adipose tissues. RESULTS There was a statistically significant difference in the weight of mice in each group after 45 and 60 d of exposure ( P < 0.05). After 60 d of exposure, the weight of liver and adipose tissues in the exposure groups were greater than that of the control group ( P < 0.05). The liver tissue structure was disordered and the liver tissues were accompanied by local inflammatory cell infiltration in the high, medium-high, and medium dose BDE-209 groups. The levels of FINS, insulin sensitivity index, Adp, and HDL-C were decreased in the BDE-209 group compared with the control group, as were the mRNA and protein levels of Adp in liver and adipose tissues ( P < 0.05). Serum level of FBG and LEP were higher in the BDE-209 group than in controls. TC, TG, and LDL-C levels as well as the mRNA and protein expression of LEP and PPARγ in liver and adipose tissues were higher than those in the control group ( P < 0.05). Homeostatic assessment model of IR was higher in the medium and medium-low dose BDE-209 groups ( P < 0.05). CONCLUSION BDE-209 increases the body weight, fat and liver tissue weight, TC, TG, and LDL-C, reduces HDL-C, and causes IR in mice, which may be related to activating the PPARγ receptor.

show abstract

Apigenin Attenuates Inflammation in Experimentally Induced Acute Pancreatitis-Associated Lung Injury

Cited by 11 publications

References 22 publications

Protective effects of ulinastatin on rats with acute lung injury induced by lipopolysaccharide

Protective effects of ulinastatin on rats with acute lung injury induced by lipopolysaccharide

Chronic Pancreatitis Associated Acute Respiratory Failure

Decabromodiphenyl ether causes insulin resistance and glucose and lipid metabolism disorders in mice

Contact Info

Product

Resources

About